Hirano Tomoko, Munnik Teun, Sato Masa H
Laboratory of Cellular Dynamics, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto 606-8522, Japan (T.H., M.H.S.); andSection Plant Physiology, Swammerdam Institute for Life Sciences, University of Amsterdam, 1098 XH Amsterdam, The Netherlands (T.M.).
Laboratory of Cellular Dynamics, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto 606-8522, Japan (T.H., M.H.S.); andSection Plant Physiology, Swammerdam Institute for Life Sciences, University of Amsterdam, 1098 XH Amsterdam, The Netherlands (T.M.)
Plant Physiol. 2015 Nov;169(3):1961-74. doi: 10.1104/pp.15.01368. Epub 2015 Sep 9.
Phosphatidylinositol 3,5-bisphosphate [PtdIns(3,5)P2] is an important lipid in membrane trafficking in animal and yeast systems; however, its role is still largely obscure in plants. Here, we demonstrate that the phosphatidylinositol 3-phosphate 5-kinase, formation of aploid and binucleate cells1 (FAB1)/FYVE finger-containing phosphoinositide kinase (PIKfyve), and its product, PtdIns(3,5)P2, are essential for the maturation process of endosomes to mediate cortical microtubule association of endosomes, thereby controlling proper PIN-FORMED protein trafficking in young cortical and stele cells of root. We found that FAB1 predominantly localizes on the Sorting Nexin1 (SNX1)-residing late endosomes, and a loss of FAB1 function causes the release of late endosomal proteins, Ara7, and SNX1 from the endosome membrane, indicating that FAB1, or its product PtdIns(3,5)P2, mediates the maturation process of the late endosomes. We also found that loss of FAB1 function causes the release of endosomes from cortical microtubules and disturbs proper cortical microtubule organization.
磷脂酰肌醇3,5 - 二磷酸[PtdIns(3,5)P2]是动物和酵母系统中膜运输过程中的一种重要脂质;然而,其在植物中的作用仍 largely obscure。在这里,我们证明磷脂酰肌醇3 - 磷酸5 - 激酶、单倍体和双核细胞形成1(FAB1)/含FYVE结构域的磷酸肌醇激酶(PIKfyve)及其产物PtdIns(3,5)P2对于内体的成熟过程至关重要,以介导内体与皮层微管的结合,从而控制根中幼嫩皮层和中柱细胞中PIN形成蛋白的正确运输。我们发现FAB1主要定位于驻留分选连接蛋白1(SNX1)的晚期内体上,FAB1功能的丧失会导致晚期内体蛋白、Ara7和SNX1从内体膜上释放,这表明FAB1或其产物PtdIns(3,5)P2介导晚期内体的成熟过程。我们还发现FAB1功能的丧失会导致内体从皮层微管上释放,并扰乱皮层微管的正常组织。